MED-NERD

Etiology and Pathophysiology of Crush Syndrome

Etiology of crush syndrome:

Crush syndrome is mainly due to crush injury or compression with heavy weight or collapse such as:

-Natural disasters like earthquakes >> structural collapse for more than 24 hours is associated with high mortality rate. About 20% of earthquake victims have crush injuries due to entrapment and building collapse.
-Accidents, whether constructural, industrial, agricultural, or vehicular accidents (being trapped under a vehicle).
-Wars (being trapped under a bombed building).
-Stampede >> crush injuries and traumatic asphyxia may occur in mass crowd stampedes.

Pathophysiology of crush syndrome:

About 80% of crush injury mortality rate is due to asphyxia or head injuries and trauma. About 10% out of the 20% that reach the hospital can make recovery. The rest of patients representing the remaining 10% of crush injury cases develop crush syndrome that is associated with severe metabolic and electrolyte disturbances.


Due to rupture of muscles in crush injury, myoglobin become released from the muscle cells into the circulation. Later it becomes converted into methmyoglobin, and eventually into acid haematin that passes into the circulation. Other components of muscle cells that are toxic become released into the circulation such as phosphate, potassium, magnesium, acids, and enzymes including lactate dehydrogenase (LDH) and creatine phosphokinase (CKMM). ATP and CK become exhausted. Calcium, sodium, and fluids become released into the muscle increasing the tension and volume of muscles. This is due to ischemia of muscles as a result of crush injury occluding the circulations of the muscles. Activation of nitric oxide system also causes vasodilation in the muscles and hypotension.

When victims become rescued and once the tension become released, disruption of sodium-potassium-ATPase pump due to correction of ischemia and reperfusion of muscles. Multiple components become released into the circulation including ions (potassium, calcium, phosphate), muscle enzymes (aldolase, creatinine phosphokinase), myoglobin degradation products, uric acid, and lactic acid.
When myoglobin exceeds the renal threshold and the filtration rate of the glomeruli, it becomes precipitated in the distal convoluted tubules leading to their obstruction. Moreover, myoglobin degradation products lead to vasoconstriction of the afferent arterioles which contributes to the destruction of tubules. The serum creatinine phosphokinase is considered the most important indicator of muscle damage. Muscle ischemia and elevated lactic acid levels are proportional to each other. The gross changes of muscle include swelling, hardness, cold, insensitivity, and necrosis of affected muscles.

Kidney damage and oliguria is not coordinated with the severity of muscle damage and injury. The kidney become oedematous. Cardiac dysrhythmias occur due to releasing potassium into the circulation. Metabolic and electrolyte disturbance eventually lead to shock. Lung oedema occur which deteriorates lung functions and gas exchange leading to Adult Respiratory Distress Syndrome (ARDS).

Although crush injuries are not common after chest and head injuries, some studies showed about 10% of chest traumas are associated with crush injuries. Crush syndrome is usually due to prolonged pressure that results in death in most cases.

Direct tissue damage and occlusion of venous circulation occur due to the compressive force. Myonecrosis (cellular death) occur leading to crush syndrome. Death occurs within 20 minutes of rescue due to sudden arrest from ventricular fibrillation which occurs due to potassium, myoglobin, and phosphorus release in the area of injury. The patient dies smiling after rescue which is known as "smiling death".